Mapping quantitative trait loci for behavioral traits in the mouse
Abstract After many years of studying various behavioral characters in the mouse, it is clear that most are heritable and are specified by complexes of genes or quantitative trait loci (QTLs). In order to attain a more complete understanding of the genetic causes of individual differences in behavio...
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E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
1992 |
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| Umfang: |
19 |
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Springer Online Journal Archives 1860-2002 |
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| Übergeordnetes Werk: |
in: Behavior genetics - 1970, 22(1992) vom: Juni, Seite 635-653 |
| Übergeordnetes Werk: |
volume:22 ; year:1992 ; month:06 ; pages:635-653 ; extent:19 |
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| 520 | |a Abstract After many years of studying various behavioral characters in the mouse, it is clear that most are heritable and are specified by complexes of genes or quantitative trait loci (QTLs). In order to attain a more complete understanding of the genetic causes of individual differences in behavior, the mechanism of action of these QTLs must be elucidated. The most straightforward approach to determining the mechanism of action of a particular QTL is to identify and molecularly clone the gene; this can be done by positional cloning, which depends on precise knowledge of the genetic map position. As the genetic data base for the mouse genome continues to develop, such strategies will become increasingly easy to perform. Here we suggest a multistage strategy for QTL mapping using recombinant-inbred strains of mice: (1) characterize genomic DNA from parental strains originally used to generate the RI strains; (2) characterize the RI strains for a quantitative character and for DNA markers that differ in the parental strains; and (3) assess the quantitative character in F2 mice derived from crosses between the parental strains, then determine the genotypes of extreme F2 mice for markers that account for at least 5% of the additive genetic variance. Data from these F2 crosses can be used to test hypotheses from the analysis of RI strains, i.e., that a QTL maps to a particular region. Using data from the mouse genome data base, this strategy should allow the molecular identification of the gene based on a candidate-gene approach. We illustrate the approach with examples from our work in mapping QTLs specifying neural sensitivity to the anesthetic effects of ethanol. | ||
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(DE-627)NLEJ196671469 DE-627 ger DE-627 rakwb eng Mapping quantitative trait loci for behavioral traits in the mouse 1992 19 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract After many years of studying various behavioral characters in the mouse, it is clear that most are heritable and are specified by complexes of genes or quantitative trait loci (QTLs). In order to attain a more complete understanding of the genetic causes of individual differences in behavior, the mechanism of action of these QTLs must be elucidated. The most straightforward approach to determining the mechanism of action of a particular QTL is to identify and molecularly clone the gene; this can be done by positional cloning, which depends on precise knowledge of the genetic map position. As the genetic data base for the mouse genome continues to develop, such strategies will become increasingly easy to perform. Here we suggest a multistage strategy for QTL mapping using recombinant-inbred strains of mice: (1) characterize genomic DNA from parental strains originally used to generate the RI strains; (2) characterize the RI strains for a quantitative character and for DNA markers that differ in the parental strains; and (3) assess the quantitative character in F2 mice derived from crosses between the parental strains, then determine the genotypes of extreme F2 mice for markers that account for at least 5% of the additive genetic variance. Data from these F2 crosses can be used to test hypotheses from the analysis of RI strains, i.e., that a QTL maps to a particular region. Using data from the mouse genome data base, this strategy should allow the molecular identification of the gene based on a candidate-gene approach. We illustrate the approach with examples from our work in mapping QTLs specifying neural sensitivity to the anesthetic effects of ethanol. Springer Online Journal Archives 1860-2002 Johnson, Thomas E. oth DeFries, John C. oth Markel, Paul D. oth in Behavior genetics 1970 22(1992) vom: Juni, Seite 635-653 (DE-627)NLEJ188995994 (DE-600)2014974-8 1573-3297 nnns volume:22 year:1992 month:06 pages:635-653 extent:19 http://dx.doi.org/10.1007/BF01066635 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 22 1992 6 635-653 19 |
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(DE-627)NLEJ196671469 DE-627 ger DE-627 rakwb eng Mapping quantitative trait loci for behavioral traits in the mouse 1992 19 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract After many years of studying various behavioral characters in the mouse, it is clear that most are heritable and are specified by complexes of genes or quantitative trait loci (QTLs). In order to attain a more complete understanding of the genetic causes of individual differences in behavior, the mechanism of action of these QTLs must be elucidated. The most straightforward approach to determining the mechanism of action of a particular QTL is to identify and molecularly clone the gene; this can be done by positional cloning, which depends on precise knowledge of the genetic map position. As the genetic data base for the mouse genome continues to develop, such strategies will become increasingly easy to perform. Here we suggest a multistage strategy for QTL mapping using recombinant-inbred strains of mice: (1) characterize genomic DNA from parental strains originally used to generate the RI strains; (2) characterize the RI strains for a quantitative character and for DNA markers that differ in the parental strains; and (3) assess the quantitative character in F2 mice derived from crosses between the parental strains, then determine the genotypes of extreme F2 mice for markers that account for at least 5% of the additive genetic variance. Data from these F2 crosses can be used to test hypotheses from the analysis of RI strains, i.e., that a QTL maps to a particular region. Using data from the mouse genome data base, this strategy should allow the molecular identification of the gene based on a candidate-gene approach. We illustrate the approach with examples from our work in mapping QTLs specifying neural sensitivity to the anesthetic effects of ethanol. Springer Online Journal Archives 1860-2002 Johnson, Thomas E. oth DeFries, John C. oth Markel, Paul D. oth in Behavior genetics 1970 22(1992) vom: Juni, Seite 635-653 (DE-627)NLEJ188995994 (DE-600)2014974-8 1573-3297 nnns volume:22 year:1992 month:06 pages:635-653 extent:19 http://dx.doi.org/10.1007/BF01066635 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 22 1992 6 635-653 19 |
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(DE-627)NLEJ196671469 DE-627 ger DE-627 rakwb eng Mapping quantitative trait loci for behavioral traits in the mouse 1992 19 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract After many years of studying various behavioral characters in the mouse, it is clear that most are heritable and are specified by complexes of genes or quantitative trait loci (QTLs). In order to attain a more complete understanding of the genetic causes of individual differences in behavior, the mechanism of action of these QTLs must be elucidated. The most straightforward approach to determining the mechanism of action of a particular QTL is to identify and molecularly clone the gene; this can be done by positional cloning, which depends on precise knowledge of the genetic map position. As the genetic data base for the mouse genome continues to develop, such strategies will become increasingly easy to perform. Here we suggest a multistage strategy for QTL mapping using recombinant-inbred strains of mice: (1) characterize genomic DNA from parental strains originally used to generate the RI strains; (2) characterize the RI strains for a quantitative character and for DNA markers that differ in the parental strains; and (3) assess the quantitative character in F2 mice derived from crosses between the parental strains, then determine the genotypes of extreme F2 mice for markers that account for at least 5% of the additive genetic variance. Data from these F2 crosses can be used to test hypotheses from the analysis of RI strains, i.e., that a QTL maps to a particular region. Using data from the mouse genome data base, this strategy should allow the molecular identification of the gene based on a candidate-gene approach. We illustrate the approach with examples from our work in mapping QTLs specifying neural sensitivity to the anesthetic effects of ethanol. Springer Online Journal Archives 1860-2002 Johnson, Thomas E. oth DeFries, John C. oth Markel, Paul D. oth in Behavior genetics 1970 22(1992) vom: Juni, Seite 635-653 (DE-627)NLEJ188995994 (DE-600)2014974-8 1573-3297 nnns volume:22 year:1992 month:06 pages:635-653 extent:19 http://dx.doi.org/10.1007/BF01066635 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 22 1992 6 635-653 19 |
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(DE-627)NLEJ196671469 DE-627 ger DE-627 rakwb eng Mapping quantitative trait loci for behavioral traits in the mouse 1992 19 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract After many years of studying various behavioral characters in the mouse, it is clear that most are heritable and are specified by complexes of genes or quantitative trait loci (QTLs). In order to attain a more complete understanding of the genetic causes of individual differences in behavior, the mechanism of action of these QTLs must be elucidated. The most straightforward approach to determining the mechanism of action of a particular QTL is to identify and molecularly clone the gene; this can be done by positional cloning, which depends on precise knowledge of the genetic map position. As the genetic data base for the mouse genome continues to develop, such strategies will become increasingly easy to perform. Here we suggest a multistage strategy for QTL mapping using recombinant-inbred strains of mice: (1) characterize genomic DNA from parental strains originally used to generate the RI strains; (2) characterize the RI strains for a quantitative character and for DNA markers that differ in the parental strains; and (3) assess the quantitative character in F2 mice derived from crosses between the parental strains, then determine the genotypes of extreme F2 mice for markers that account for at least 5% of the additive genetic variance. Data from these F2 crosses can be used to test hypotheses from the analysis of RI strains, i.e., that a QTL maps to a particular region. Using data from the mouse genome data base, this strategy should allow the molecular identification of the gene based on a candidate-gene approach. We illustrate the approach with examples from our work in mapping QTLs specifying neural sensitivity to the anesthetic effects of ethanol. Springer Online Journal Archives 1860-2002 Johnson, Thomas E. oth DeFries, John C. oth Markel, Paul D. oth in Behavior genetics 1970 22(1992) vom: Juni, Seite 635-653 (DE-627)NLEJ188995994 (DE-600)2014974-8 1573-3297 nnns volume:22 year:1992 month:06 pages:635-653 extent:19 http://dx.doi.org/10.1007/BF01066635 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 22 1992 6 635-653 19 |
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(DE-627)NLEJ196671469 DE-627 ger DE-627 rakwb eng Mapping quantitative trait loci for behavioral traits in the mouse 1992 19 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract After many years of studying various behavioral characters in the mouse, it is clear that most are heritable and are specified by complexes of genes or quantitative trait loci (QTLs). In order to attain a more complete understanding of the genetic causes of individual differences in behavior, the mechanism of action of these QTLs must be elucidated. The most straightforward approach to determining the mechanism of action of a particular QTL is to identify and molecularly clone the gene; this can be done by positional cloning, which depends on precise knowledge of the genetic map position. As the genetic data base for the mouse genome continues to develop, such strategies will become increasingly easy to perform. Here we suggest a multistage strategy for QTL mapping using recombinant-inbred strains of mice: (1) characterize genomic DNA from parental strains originally used to generate the RI strains; (2) characterize the RI strains for a quantitative character and for DNA markers that differ in the parental strains; and (3) assess the quantitative character in F2 mice derived from crosses between the parental strains, then determine the genotypes of extreme F2 mice for markers that account for at least 5% of the additive genetic variance. Data from these F2 crosses can be used to test hypotheses from the analysis of RI strains, i.e., that a QTL maps to a particular region. Using data from the mouse genome data base, this strategy should allow the molecular identification of the gene based on a candidate-gene approach. We illustrate the approach with examples from our work in mapping QTLs specifying neural sensitivity to the anesthetic effects of ethanol. Springer Online Journal Archives 1860-2002 Johnson, Thomas E. oth DeFries, John C. oth Markel, Paul D. oth in Behavior genetics 1970 22(1992) vom: Juni, Seite 635-653 (DE-627)NLEJ188995994 (DE-600)2014974-8 1573-3297 nnns volume:22 year:1992 month:06 pages:635-653 extent:19 http://dx.doi.org/10.1007/BF01066635 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 22 1992 6 635-653 19 |
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Mapping quantitative trait loci for behavioral traits in the mouse |
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Abstract After many years of studying various behavioral characters in the mouse, it is clear that most are heritable and are specified by complexes of genes or quantitative trait loci (QTLs). In order to attain a more complete understanding of the genetic causes of individual differences in behavior, the mechanism of action of these QTLs must be elucidated. The most straightforward approach to determining the mechanism of action of a particular QTL is to identify and molecularly clone the gene; this can be done by positional cloning, which depends on precise knowledge of the genetic map position. As the genetic data base for the mouse genome continues to develop, such strategies will become increasingly easy to perform. Here we suggest a multistage strategy for QTL mapping using recombinant-inbred strains of mice: (1) characterize genomic DNA from parental strains originally used to generate the RI strains; (2) characterize the RI strains for a quantitative character and for DNA markers that differ in the parental strains; and (3) assess the quantitative character in F2 mice derived from crosses between the parental strains, then determine the genotypes of extreme F2 mice for markers that account for at least 5% of the additive genetic variance. Data from these F2 crosses can be used to test hypotheses from the analysis of RI strains, i.e., that a QTL maps to a particular region. Using data from the mouse genome data base, this strategy should allow the molecular identification of the gene based on a candidate-gene approach. We illustrate the approach with examples from our work in mapping QTLs specifying neural sensitivity to the anesthetic effects of ethanol. |
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Abstract After many years of studying various behavioral characters in the mouse, it is clear that most are heritable and are specified by complexes of genes or quantitative trait loci (QTLs). In order to attain a more complete understanding of the genetic causes of individual differences in behavior, the mechanism of action of these QTLs must be elucidated. The most straightforward approach to determining the mechanism of action of a particular QTL is to identify and molecularly clone the gene; this can be done by positional cloning, which depends on precise knowledge of the genetic map position. As the genetic data base for the mouse genome continues to develop, such strategies will become increasingly easy to perform. Here we suggest a multistage strategy for QTL mapping using recombinant-inbred strains of mice: (1) characterize genomic DNA from parental strains originally used to generate the RI strains; (2) characterize the RI strains for a quantitative character and for DNA markers that differ in the parental strains; and (3) assess the quantitative character in F2 mice derived from crosses between the parental strains, then determine the genotypes of extreme F2 mice for markers that account for at least 5% of the additive genetic variance. Data from these F2 crosses can be used to test hypotheses from the analysis of RI strains, i.e., that a QTL maps to a particular region. Using data from the mouse genome data base, this strategy should allow the molecular identification of the gene based on a candidate-gene approach. We illustrate the approach with examples from our work in mapping QTLs specifying neural sensitivity to the anesthetic effects of ethanol. |
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Abstract After many years of studying various behavioral characters in the mouse, it is clear that most are heritable and are specified by complexes of genes or quantitative trait loci (QTLs). In order to attain a more complete understanding of the genetic causes of individual differences in behavior, the mechanism of action of these QTLs must be elucidated. The most straightforward approach to determining the mechanism of action of a particular QTL is to identify and molecularly clone the gene; this can be done by positional cloning, which depends on precise knowledge of the genetic map position. As the genetic data base for the mouse genome continues to develop, such strategies will become increasingly easy to perform. Here we suggest a multistage strategy for QTL mapping using recombinant-inbred strains of mice: (1) characterize genomic DNA from parental strains originally used to generate the RI strains; (2) characterize the RI strains for a quantitative character and for DNA markers that differ in the parental strains; and (3) assess the quantitative character in F2 mice derived from crosses between the parental strains, then determine the genotypes of extreme F2 mice for markers that account for at least 5% of the additive genetic variance. Data from these F2 crosses can be used to test hypotheses from the analysis of RI strains, i.e., that a QTL maps to a particular region. Using data from the mouse genome data base, this strategy should allow the molecular identification of the gene based on a candidate-gene approach. We illustrate the approach with examples from our work in mapping QTLs specifying neural sensitivity to the anesthetic effects of ethanol. |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ196671469</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20210705194413.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">070526s1992 xx |||||o 00| ||eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ196671469</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Mapping quantitative trait loci for behavioral traits in the mouse</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1992</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">19</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract After many years of studying various behavioral characters in the mouse, it is clear that most are heritable and are specified by complexes of genes or quantitative trait loci (QTLs). In order to attain a more complete understanding of the genetic causes of individual differences in behavior, the mechanism of action of these QTLs must be elucidated. The most straightforward approach to determining the mechanism of action of a particular QTL is to identify and molecularly clone the gene; this can be done by positional cloning, which depends on precise knowledge of the genetic map position. As the genetic data base for the mouse genome continues to develop, such strategies will become increasingly easy to perform. Here we suggest a multistage strategy for QTL mapping using recombinant-inbred strains of mice: (1) characterize genomic DNA from parental strains originally used to generate the RI strains; (2) characterize the RI strains for a quantitative character and for DNA markers that differ in the parental strains; and (3) assess the quantitative character in F2 mice derived from crosses between the parental strains, then determine the genotypes of extreme F2 mice for markers that account for at least 5% of the additive genetic variance. Data from these F2 crosses can be used to test hypotheses from the analysis of RI strains, i.e., that a QTL maps to a particular region. Using data from the mouse genome data base, this strategy should allow the molecular identification of the gene based on a candidate-gene approach. We illustrate the approach with examples from our work in mapping QTLs specifying neural sensitivity to the anesthetic effects of ethanol.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="f">Springer Online Journal Archives 1860-2002</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Johnson, Thomas E.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">DeFries, John C.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Markel, Paul D.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">in</subfield><subfield code="t">Behavior genetics</subfield><subfield code="d">1970</subfield><subfield code="g">22(1992) vom: Juni, Seite 635-653</subfield><subfield code="w">(DE-627)NLEJ188995994</subfield><subfield code="w">(DE-600)2014974-8</subfield><subfield code="x">1573-3297</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:22</subfield><subfield code="g">year:1992</subfield><subfield code="g">month:06</subfield><subfield code="g">pages:635-653</subfield><subfield code="g">extent:19</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1007/BF01066635</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-SOJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">22</subfield><subfield code="j">1992</subfield><subfield code="c">6</subfield><subfield code="h">635-653</subfield><subfield code="g">19</subfield></datafield></record></collection>
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